MicroRNA-24 Regulates Macrophage Behavior and Retards Atherosclerosis

Abstract

Taken together, our data demonstrates that downregulation of microRNA-24 promotes an invasive macrophage subset and plays a novel regulatory role in MMP-14 proteolytic activity and, therefore, plaque stability, highlighting its therapeutic potential.

MicroRNA‑24 inhibits the proliferation and migration of endothelial cells in patients with atherosclerosis by targeting importin‑α3 and regulating inflammatory responses

“…The most important processes in the occurrence and development of atherosclerosis include i) vascular endothelial cell injury and inflammatory activation; ii) the proliferation and migration of endothelial/smooth muscle cells; and iii) the release of inflammatory mediators stimulated by macrophage activation (27)(28)(29)(30). It has been reported that miR-24 expression is downregulated in atherosclerotic plaques, and miR-24 participates in the formation of atherosclerosis primarily by targeting and inhibiting matrix metalloproteinase-14 (31). In the present study, it was demonstrated that miR-24 expression is significantly lower in patients with atherosclerosis, as compared with healthy subjects.…”

MicroRNA Regulation of Vascular Smooth Muscle Function and Phenotype

“…49 Interestingly, miR-24 has furthermore been shown to regulate the activation of vascular disease-associated macrophages and atherosclerosis retardation. 50 miR-29, however, has been identified as an important regulator of extracellular matrix remodeling and the fibrotic response in cardiovascular disease, 51 with its inhibition being able toamong other mechanisms-effectively restore elastin levels in fibroblasts and SMCs. 52 Another microRNA with an effect on VSMC biology and vascular remodeling is miR-26a.…”

Pioglitazone Increases Circulating MicroRNA-24 With Decrease in Coronary Neointimal Hyperplasia in Type 2 Diabetic Patients – Optical Coherence Tomography Analysis –

“…12-18 Expression of endothelial microRNA-24 reduces the organization of actin into stress fiber, thereby decreasing cell migration; 18 furthermore, stable plaque expresses higher microRNA-24 than unstable plaque. 18, 19 We prospectively compared the effects of pioglitazone in neointimal hyperplasia after coronary stenting and the changes in circulating microRNA-17,-24,-92a,-126,-145 with neointimal hyperplasia status in type 2 diabetic patients during 9-month follow-up.…”